Polymicrogyria in fetal alcohol syndrome

Reinhardt, K; Mohr, Alexander T.; Gärtner, Jutta; Spohr, Hans‐Ludwig; Brockmann, Knut

doi:10.1002/bdra.20629

Cited by 20 publications

(11 citation statements)

References 44 publications

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“…Our study did not use the same methodological approach but rather used a more exploratory technique to examine gyrification at thousands of points over the entire cortical surface. Atypical gyrification has also been noted in case studies, which documented polymicrogyria in individuals prenatally exposed to alcohol (Clarren, Alvord, Sumi, Streissguth, & Smith, 1978; Peiffer, Majewski, Fischbach, Bierich, & Volk, 1979; Reinhardt, Mohr, Gartner, Spohr, & Brockmann, 2010). …”

Section: Discussionmentioning

confidence: 79%

Atypical cortical gyrification in adolescents with histories of heavy prenatal alcohol exposure

et al. 2015

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Prenatal alcohol exposure can adversely affect brain development, although little is known about the effects of prenatal alcohol exposure on gyrification. Gyrification reflects cortical folding complexity and is a process by which the surface of the brain creates sulci and gyri. Prior studies have shown that prenatal alcohol exposure is associated with reduced gyrification in childhood, but no studies have examined adolescents. Subjects (12–16y) comprised two age-equivalent groups: 30 adolescents with histories of heavy prenatal alcohol exposure (AE) and 19 non-exposed controls (CON). A T1-weighted image was obtained for all participants. Local gyrification index (LGI) was estimated using FreeSurfer. General linear models were used to determine between group differences in LGI controlling for age and sex. Age-by-group interactions were also investigated while controlling for sex. The AE group displayed reduced LGI relative to CON in the bilateral superior parietal region, right postcentral region, and left precentral and lateral occipital regions (ps < .001). Significant age-by-group interactions were observed in the right precentral and lateral occipital regions, and in the left pars opercularis and inferior parietal regions (ps < .01). The AE group showed age-related reductions in gyrification in all regions whereas the CON group showed increased gyrification with age in the lateral occipital region only. While cross-sectional, the age-related reduction in gyrification observed in the AE group suggests alterations in cortical development throughout adolescence and provides further insight into the pathophysiology and brain maturation of adolescents prenatally exposed to alcohol.

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Section: Discussionmentioning

confidence: 79%

Atypical cortical gyrification in adolescents with histories of heavy prenatal alcohol exposure

et al. 2015

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“…Other studies in this mouse model have demonstrated that right eyes and limbs are affected by early gestational ethanol exposure nearly twice as often as the left (Chen, et al, 2004; Cook, et al, 1987; Parnell, et al, 2006). Asymmetries have also been observed in many patients with FAS, as documented in reports of disproportionate reductions in the size of the left hippocampus and frontal lobes, along with alterations in the normal cortical gray matter patterns (Reinhardt, et al, 2010; Riikonen, et al, 1999; Sowell, et al, 2001; Sowell, et al, 2002). In addition to the brain, the craniofacies of individuals with FAS may be asymmetric.…”

Section: Discussionmentioning

confidence: 83%

Magnetic resonance microscopy-based analyses of the neuroanatomical effects of gestational day 9 ethanol exposure in mice

Parnell

Holloway

O’Leary‐Moore

et al. 2013

Neurotoxicology and Teratology

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Animal model-based studies have shown that ethanol exposure during early gestation induces developmental stage-specific abnormalities of the face and brain. The exposure time-dependent variability in ethanol’s teratogenic outcomes is expected to contribute significantly to the wide spectrum of effects observed in humans with fetal alcohol spectrum disorder (FASD). The work presented here employs a mouse FASD model and magnetic resonance microscopy (MRM; high resolution magnetic resonance imaging) in studies designed to further our understanding of the developmental stage-specific defects of the brain that are induced by ethanol. At neurulation stages, i.e. at the beginning of gestational day (GD) 9 and again 4 hours later, time-mated C57Bl/6J dams were intraperitoneally administered 2.9 g/kg ethanol or vehicle. Ethanol-exposed fetuses were collected on GD 17, processed for MRM analysis, and results compared to comparably staged controls. Linear and volume measurements as well as shape changes for numerous individual brain regions were determined. GD 9 ethanol exposure resulted in significantly increased septal region width, reduction of cerebellar volume, and enlargement of all of the ventricles. Additionally, the results of shape analyses showed that many areas of the ethanol-exposed brains including the cerebral cortex, hippocampus and right striatum were significantly misshapen. These data demonstrate that ethanol can induce dysmorphology that may not be obvious based on volumetric analyses alone, highlight the asymmetric aspects of ethanol-induced defects, and add to our understanding of ethanol’s developmental stage-dependent neuroteratogenesis.

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“…For example, previous research has shown that cortical folding affects later functional development (Dubois et al, 2008) in a manner that affects intelligence. Polymicrogyria (an abnormality in neuronal migration that results in an increase in the number of gyri) has been observed in a 16 year old female with PAE who met full FAS diagnostic criteria (Reinhardt et al, 2010). Reinhardt and colleagues suggested that FAS should, in fact, be considered as part of the differential diagnosis process in cases where polymicrogyria has been identified.…”

Section: Discussionmentioning

confidence: 99%

Cortical gyrification is abnormal in children with prenatal alcohol exposure

Hendrickson

Mueller

Sowell

et al. 2017

NeuroImage: Clinical

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ObjectivesPrenatal alcohol exposure (PAE) adversely affects early brain development. Previous studies have shown a wide range of structural and functional abnormalities in children and adolescents with PAE. The current study adds to the existing literature specifically on cortical development by examining cortical gyrification in a large sample of children with PAE compared to controls. Relationships between cortical development and intellectual functioning are also examined.Experimental designIncluded were 92 children with PAE and 83 controls ages 9–16 from four sites in the Collaborative Initiative on FASD (CIFASD). All PAE participants had documented heavy PAE. All underwent a formal evaluation of physical anomalies and dysmorphic facial features. MRI data were collected using modified matched protocols on three platforms (Siemens, GE, and Philips). Cortical gyrification was examined using a semi-automated procedure.Principal observationsWhole brain group comparisons using Monte Carlo z-simulation for multiple comparisons showed significantly lower cortical gyrification across a large proportion of the cerebral cortex amongst PAE compared to controls. Whole brain comparisons and ROI based analyses showed strong positive correlations between cortical gyrification and IQ (i.e. less developed cortex was associated with lower IQ).ConclusionsAbnormalities in cortical development were seen across the brain in children with PAE compared to controls. Cortical gyrification and IQ were strongly correlated, suggesting that examining mechanisms by which alcohol disrupts cortical formation may yield clinically relevant insights and potential directions for early intervention.

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Polymicrogyria in fetal alcohol syndrome

Cited by 20 publications

References 44 publications

Atypical cortical gyrification in adolescents with histories of heavy prenatal alcohol exposure

Atypical cortical gyrification in adolescents with histories of heavy prenatal alcohol exposure

Magnetic resonance microscopy-based analyses of the neuroanatomical effects of gestational day 9 ethanol exposure in mice

Cortical gyrification is abnormal in children with prenatal alcohol exposure

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